牙周炎与动脉粥样硬化信号相互作用的关联影响
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摘要
我国65岁以上的老年人牙周炎发病率高达70%以上,近年来随着饮食结构改变,动脉粥样硬化的发病率有逐年升高及年轻化的趋势,大量研究结果显示,慢性牙周炎与动脉粥样硬化之间有共同的风险因素。动脉粥样硬化是心血管疾病主要病因,炎症反应是动脉粥样硬化斑块形成的重要始动因素,而慢性牙周炎作为由微生物引起的慢性多因子炎症性疾病,与动脉粥样硬化的发生有着密不可分的联系。在牙周致病菌中牙龈卟啉单胞菌为慢性牙周炎的主要致病菌,相关毒素可穿过牙龈上皮等进入血液循环,通过长期慢性刺激导致血管内皮细胞功能障碍和激活血液中炎症因子,最终促进血管内斑块的形成。本文简要阐述牙周炎与动脉粥样硬化之间的相关性。
The incidence of chronic periodontitis(CP)is over 70%in the over 65 years old people in China.And the prevalence of atherosclerosis(AS)is increasing with the change of dietary structure.A large number of studies reported that there are common risk factors between CP and AS.CP,a chronic multi-factor inflammatory disease caused by microorganisms,is closely related to AS which is based on chronic infection and is a key basic pathological of cardiovascular disease.Porphyromonas gingivalis(P.g.)is a main periodontal pathogen to CP.From gingival epithelium,P.g.enters the bloodstream,which causes the endothelial dysfunction,releases the inflammatory cytokines,turns macrophages phagocytose lipids into foam cells,and causes the formation of atheroslerotic plaque.This article discussed the association between CP and AS.
The incidence of chronic periodontitis(CP)is over 70%in the over 65 years old people in China.And the prevalence of atherosclerosis(AS)is increasing with the change of dietary structure.A large number of studies reported that there are common risk factors between CP and AS.CP,a chronic multi-factor inflammatory disease caused by microorganisms,is closely related to AS which is based on chronic infection and is a key basic pathological of cardiovascular disease.Porphyromonas gingivalis(P.g.)is a main periodontal pathogen to CP.From gingival epithelium,P.g.enters the bloodstream,which causes the endothelial dysfunction,releases the inflammatory cytokines,turns macrophages phagocytose lipids into foam cells,and causes the formation of atheroslerotic plaque.This article discussed the association between CP and AS.
引文
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[2]刘冬宇,丁芳,吕亚林,等.缺血性脑卒中患者龈下菌斑中牙周致病菌检测[J].中华老年口腔医学杂志,2016,14(5)∶282-286
[3]杨静,葛颂.牙龈卟啉单胞菌与动脉粥样硬化相关性的研究进展[J].中国医药导报,2017,14(6)∶37-40
[4] Chen Y,Li X,Boini KM,et al.Endothelial Nlrp3inflammasome activation associated with lysosomal destabilization during coronary arteritis[J].Biochim Biophys Acta,2015,1853(2)∶396-408
[5] Huck O,Elkaim R,Davideau JL,et al.Porphyromonas gingivalis-impaired innate immune response via NLRP3proteolysis in endothelial cells[J].Innate Immun,2015,21(1)∶65-72
[6] Bugueno IM,Khelif Y,Seelam N,et al.Porphyromonas gingivalis differentially modulates cell death profile in ox-LDL and TNF-αpre-treated endothelial Cells[J].PLoS One,2016,11(4)∶e0154590
[7]吕宗凯,郑杨灿,杜胜男,等.慢性牙周炎与脑卒中关系的Meta分析[J].中华口腔医学研究杂志(电子版),2017,11(1)∶31-35
[8] Lin M,Yang HU,Wang Y,et al.Different engagement of TLR2and TLR4in porphyromonas gingivalis vs.ligatureinduced periodontal bone loss[J].Braz Oral Res,2017,31∶e63
[9] Bhaskar S, Helen A. Quercetin modulates toll-like receptor-mediated protein kinase signaling pathways in oxLDL-challenged human PBMCs and regulates TLR-activated atherosclerotic inflammation in hypercholesterolemic rats[J].Mol Cell Biochem,2016,423(1-2)∶53-65
[10] Kigawa Y,Miyazaki T,Lei XF,et al.Functional heterogeneity of NADPH oxidases in atherosclerotic and aneurysmal diseases[J].J Atheroscler Thromb,2017,24(1)∶1-13
[11] Steyers CM,Miller FJ.Endothelial dysfunction in chronic inflammatory diseases[J].Int J Mol Sci,2014,15(7)∶11324-11349
[12] Mizrachi A,Cotrim AP,Katabi N,et al.Radiation-induced microvascular injury as a mechanism of salivary gland hypofunction and potential target for radioprotectors[J].Radiat Res,2016,186(2)∶189-195
[13] Das A,Gopalakrishnan B,Druhan L J,et al.Reversal of SIN-1-induced eNOS dysfunction by the spin trap,DMPO,in bovine aortic endothelial cells via eNOS phosphorylation[J].Brit J Pharmacol,2014,171(9)∶2321-2334
[14] Velsko IM,Chukkapalli SS,Rivera MF,et al.Active invasion of oral and aortic tissues by porphyromonas gingivalis in mice causally links periodontitis and atherosclerosis[J].PLoS One,2014,9(5)∶e97811
[15] Muniz F,Taminski K,Cavagni J,et al.The effect of statins on periodontal treatment-a systematic review with metaanalyses and meta-regression[J].Clin Oral Invest,2018,22(4)∶1-17
[16] Brito LC,DalBo S,Striechen TM,et al.Experimental periodontitis promotes transient vascular inflammation and endothelial dysfunction[J].Arch Oral Biol,2013,58(9)∶1187-1198
[17] Higashi Y,Goto C,Jitsuiki D,et al.Periodontal infection is associated with endothelial dysfunction in healthy subjects and hypertensive patients[J].Hypertension,2008,51(2)∶446-453
[18] Slowik J,Wnuk MA,Grzech K,et al.Periodontitis affects neurological deficit in acute stroke[J].J Neurol Sci,2010,297(1-2)∶82-84
[19]刘萍,兰倩,陈淑仪.牙周炎与高血压前期的相关性研究[J].临床心血管病杂志,2016,32(1)∶32-35
[20] Nordin A,Jensenurstad K,Bjornadal L,et al.Ischemic arterial events and atherosclerosis in patients with systemic sclerosis:apopulation-based case-control study[J].Arthritis Res Ther,2013,15(4)∶R87
[21]刘彦.慢性牙周炎与高血压患者免疫炎症因子水平的相关性研究[D].吉林大学,2013
[22] Schenkein HA,Sabatini R,Koertge TE,et al.Anti-cardiolipin from periodontitis patients induces MCP-1production by human umbilical vein endothelial cells[J].J Clin Periodontol,2013,40(3)∶212-217